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1
Anaerobic performance and metabolism of the hyperthyroid heart.甲状腺功能亢进性心脏的无氧运动能力与代谢
J Clin Invest. 1969 Oct;48(10):1905-13. doi: 10.1172/JCI106157.
2
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4
Studies on glycolysis in vitro: role of glucose phosphorylation and phosphofructokinase activity on total velocity.体外糖酵解研究：葡萄糖磷酸化和磷酸果糖激酶活性对总速率的作用
Int J Biochem. 1984;16(5):469-76. doi: 10.1016/0020-711x(84)90162-9.
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Anaerobic rat heart. Effects of glucose and tricarboxylic acid-cycle metabolites on metabolism and physiological performance.厌氧大鼠心脏。葡萄糖和三羧酸循环代谢产物对代谢和生理性能的影响。
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8
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Effects of regional ischemia on metabolism of glucose and fatty acids. Relative rates of aerobic and anaerobic energy production during myocardial infarction and comparison with effects of anoxia.局部缺血对葡萄糖和脂肪酸代谢的影响。心肌梗死期间有氧和无氧能量产生的相对速率以及与缺氧影响的比较。
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1
Glycolytic inhibition: effects on diastolic relaxation and intracellular calcium handling in hypertrophied rat ventricular myocytes.糖酵解抑制：对肥厚大鼠心室肌细胞舒张期松弛及细胞内钙处理的影响
J Clin Invest. 1995 Jun;95(6):2766-76. doi: 10.1172/JCI117980.
2
Exacerbation of ischemic dysfunction by angiotensin II in red cell-perfused rabbit hearts. Effects on coronary flow, contractility, and high-energy phosphate metabolism.红细胞灌注兔心脏中血管紧张素 II 对缺血性功能的加剧作用。对冠脉血流、收缩性和高能磷酸代谢的影响。
J Clin Invest. 1992 Feb;89(2):490-8. doi: 10.1172/JCI115611.
3
Irreversible myocardial injury in anoxic perfused rat hearts.缺氧灌注大鼠心脏中的不可逆性心肌损伤。
Am J Pathol. 1975 Sep;80(3):419-50.

本文引用的文献

1
Metabolic effects of thyroxine in vitro.甲状腺素的体外代谢效应。
Ann N Y Acad Sci. 1951 Dec;54(4):636-48. doi: 10.1111/j.1749-6632.1951.tb46619.x.
2
The mode of action of thyroxin.甲状腺素的作用方式。
Arch Biochem Biophys. 1951 Oct;33(3):486-7. doi: 10.1016/0003-9861(51)90137-3.
3
Enzyme responses to thyroid hormones.酶对甲状腺激素的反应。
Ann N Y Acad Sci. 1960 Apr 23;86:506-11. doi: 10.1111/j.1749-6632.1960.tb42826.x.
4
EFFECT OF THYROXINE AND THIOURACIL ON THE MG++-ACTIVATED ATPASE ON THE RAT MYOCARDIUM.甲状腺素和硫脲嘧啶对大鼠心肌中镁离子激活的ATP酶的作用。
Life Sci (1962). 1964 May;3:431-40. doi: 10.1016/0024-3205(64)90203-6.
5
The action of thyroid hormones at the cell level.甲状腺激素在细胞水平的作用。
Biochem J. 1963 Mar;86(3):408-28. doi: 10.1042/bj0860408.
6
Effects of 2-deoxyglucose on carbohydrate metablism: review of the literature and studies in the rat.2-脱氧葡萄糖对碳水化合物代谢的影响：文献综述及大鼠研究
Metabolism. 1962 Oct;11:1098-112.
7
[A simple technic for extremely rapid freezing of large pieces of tissue].[一种用于极快速冷冻大块组织的简单技术]
Pflugers Arch Gesamte Physiol Menschen Tiere. 1960;270:399-412.
8
Localization of interaction sites in multi-component transfer systems: theorems derived from analogues.多组分转移系统中相互作用位点的定位：从类似物推导的定理
Nature. 1958 Nov 1;182(4644):1190-3. doi: 10.1038/1821190a0.
9
Adenosine triphosphatase and morphological integrity of mitochondria.腺苷三磷酸酶与线粒体的形态完整性
Biochim Biophys Acta. 1957 Dec;26(3):522-5. doi: 10.1016/0006-3002(57)90099-9.
10
ATPase activity of rat liver mitochondria.大鼠肝脏线粒体的ATP酶活性
Biochim Biophys Acta. 1957 Feb;23(2):404-12. doi: 10.1016/0006-3002(57)90345-1.

甲状腺功能亢进性心脏的无氧运动能力与代谢

Anaerobic performance and metabolism of the hyperthyroid heart.

作者信息

Altschuld R A, Weiss A, Kruger F A, Weissler A M

出版信息

J Clin Invest. 1969 Oct;48(10):1905-13. doi: 10.1172/JCI106157.

DOI:10.1172/JCI106157
PMID:4241815
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC322427/
Abstract

Anaerobically periused hearts from rats with experimentally induced hyperthyroidism exhibited accelerated deterioration of pacemaker activity and ventricular performance. The diminished anaerobic performance of hyperthyroid hearts was associated with decreased adenosine triphosphate (ATP) levels and a reduced rate of anaerobic glycolysis as reflected in decreased lactic acid production during 30 min of anoxic perfusion.Studies on whole heart homogenates demonstrated inhibition at the phosphofructokinase (PFK) step of the glycolytic pathway. Such inhibition was not demonstrated in the hyperthyroid heart cytosol. It is postulated that an inhibitor of PFK which resides dominantly in the particulate fraction is probably responsible for the diminished anaerobic glycolysis and performance of the hyperthyroid heart.

摘要

对实验性诱导甲状腺功能亢进大鼠的心脏进行无氧灌注时，发现其起搏器活动和心室功能加速恶化。甲状腺功能亢进心脏的无氧功能下降与三磷酸腺苷（ATP）水平降低以及无氧糖酵解速率降低有关，这在30分钟缺氧灌注期间乳酸生成减少中得到体现。对全心脏匀浆的研究表明，糖酵解途径的磷酸果糖激酶（PFK）步骤受到抑制。而在甲状腺功能亢进心脏的细胞溶胶中未发现这种抑制作用。据推测，主要存在于颗粒部分的PFK抑制剂可能是导致甲状腺功能亢进心脏无氧糖酵解和功能下降的原因。